The extent of harmful volatile organic compounds released when smoking after breaking the flavor capsules of heat-not-burn (HNB) cigarette products.

A number of flavored capsule heat-not-burn (FC-HNB) tobacco products such as IQOS, Lil, and Glo have been introduced as a new generation of cigarettes. As they can release various types of volatile organic compounds (VOCs), it is important to assess the harmfulness associated with their use. Thus, the composition of VOCs in HNB cigarette vapor was evaluated to investigate the interactive roles of key variables controlling the relationships between VOC composition and capsule breaking, particularly the compositional changes induced by capsule breaking and release of flavor from FC-HNB cigarettes relative to regular products. As the capsules of FC-HNB cigarettes were broken, the total VOC concentrations increased by as high as eight times from 60.3 ± 0.48 to 488 ± 21.8 µg cig-1. The key VOC components released after breaking the flavored capsules were identified as ethyl butyrate (157 ± 13.6 µg cig-1; Lil), isoamyl acetate (76.9 ± 1.98 µg cig-1; Lil), and limonene (52.3 ± 3.29 µg cig-1; Glo). If the primary health risks of FC-HNB cigarette vapor are assessed using National Institute for Occupational Safety & Health (NIOSH) guidelines, 2,3-butanedinone exceeds the maximum daily intake limit (i.e., 0.05 mg day-1). Our study is expected to offer valuable insights into the harmful effects of direct and indirect exposure to various VOCs in FC-HNB products.

Comparison of cytotoxicity of cigarette smoke extract derived from heat-not-burn and combustion cigarettes in human vascular endothelial cells.

The present study compared the properties of mainstream smoke generated from heat-not-burn (HNB) cigarettes and a combustion cigarette (hi-lite™ brand). Three types of cigarette heating devices were used to generate cigarette smoke at different heating temperatures [Ploom S™ (200 °C), glo™ (240 °C), and IQOS™ (300-350 °C)]. Mainstream smoke was generated using the following puffing regimen: volume, 55 mL; duration, 3 s; and interval, 30 s. The rank order of particulate phase (nicotine and tar) amounts trapped on a Cambridge filter was Ploom S < glo < IQOS < hi-lite. Heated cigarette-derived smoke extract (hCSE) from the devices except for Ploom S, and burned CSE (bCSE) decreased mitochondrial metabolic activity (glo < IQOS < hi-lite) in human vascular endothelial cells. Furthermore, the cytotoxicity was reduced by removing the particulate phase from the mainstream smoke. Endothelial nitric oxide synthase activity was reduced by nicotine- and tar-free CSE of IQOS and hi-lite (IQOS < hi-lite), but not Ploom S and glo. These inhibitory effects were diminished by removing the carbonyl compounds from the mainstream smoke. These results indicated that the cytotoxicity of hCSE was lower than that of bCSE in vascular endothelial cells.

Profiling the Acute Effects of Modified Risk Products: Evidence from the SUR-VAPES (Sapienza University of Rome-Vascular Assessment of Proatherosclerotic Effects of Smoking) Cluster Study.

PURPOSE OF REVIEW: Modified risk products (MRP) are promoted as a safer alternative to traditional combustion cigarettes (TCC) in chronic smokers. Evidence for their lower hazardous profile is building, despite several controversies. Yet, it is unclear whether individual responses to MRP differ among consumers. We hypothesized that different clusters of subjects exist in terms of acute effects of MRP. RECENT FINDINGS: Pooling data from a total of 60 individuals, cluster analysis identified at least three clusters (labelled 1 to 3) of subjects with different electronic vaping cigarettes (EVC) effects and at least two clusters (labelled 4 to 5) of subjects with different heat-not-burn cigarettes (HNBC) effects. Specifically, oxidative stress, platelet aggregation, and endothelial dysfunction after EVC were significantly different cluster-wise (all p < 0.05), and oxidative stress and platelet aggregation after HNBC were significantly different (all p < 0.05). In particular, subjects belonging to Cluster 1 appeared to have less detrimental responses to EVC usage than subjects in Cluster 2 and 3, as shown by non-significant changes in flow-mediated dilation (FMD) and less marked increase in Nox2-derived peptide (NOX). Conversely, those assigned to Cluster 3 had the worst reaction in terms of changes in FMD, NOX, and P-selectin. Furthermore, individuals belonging to Cluster 4 responded unfavorably to both HNBC and EVC, whereas those in Cluster 5 interestingly showed less adverse results after using HNBC than EVC. Results for main analyses were consistent employing different clusters, tests, and bootstrap. Individual responses to MRP differ and smokers aiming at using EVC or HNBC as a risk reduction strategy should consider trying different MRP aiming at finding the one which is less detrimental, with subjects resembling those in Cluster 1 preferably using EVC and those resembling Cluster 5 preferably using HNBC.

Sex-Related Differences in Oxidative, Platelet, and Vascular Function in Chronic Users of Heat-not-Burn vs. Traditional Combustion Cigarettes.

Smoking is still a major cardiovascular risk factor, despite many public awareness campaigns and dedicated interventions. Recently, modified risk products (MRP), e.g., heat-not-burn cigarettes (HNBCs), have been introduced as surrogates of traditional combustion cigarettes (TCCs). Although these products are promoted as healthier than TCCs, few studies have been conducted to assess it. This work is a sex-focused sub-study of a prospective observational study in which apparently healthy chronic TCC smokers were age-matched with regular HNBC users. Blood samples were collected for biochemical assays and blood pressure and flow-mediated dilation (FMD) were measured. Out of 60 subjects, 33 (55%) were women, and 27 (45%) men, with 11 (33%) vs. 9 (33%) non-smokers, respectively, 10 (30%) vs. 10 (37%) TCC smokers, and 12 (36%) vs. 8 (30%) HNBC smokers (p = 0.946). Bivariate and multivariable analyses showed no statistically significant between-sex differences in NO, H2O2, sCD40L, sNox2-dp, sP-selectin, platelet aggregation, cotinine or FMD, overall, in non-smokers, in TCC smokers, or in HNBC smokers (all p > 0.05). HNBCs appeared safer than TCCs when focusing on Nox2-dp (p = 0.026) and sP-selectin (p = 0.050) but had similar levels of the other measured markers. In conclusion, HNBCs have similar detrimental effects on women and men's oxidative stress (H2O2: p = 0.49; sNox2-dp: p = 0.31) and platelet activation (sP-selectin: p = 0.33; platelet aggregation p = 0.87).

Comparison of Nicotine Dependence and Biomarker Levels among Traditional Cigarette, Heat-Not-Burn Cigarette, and Liquid E-Cigarette Users: Results from the Think Study.

This study aimed to compare Korean smokers' smoking-related biomarker levels by tobacco product type, including heat-not-burn cigarettes (HNBC), liquid e-cigarettes (EC), and traditional cigarettes (TC). Nicotine dependence levels were evaluated in Korean adult study participants including TC-, EC-, HNBC-only users and nonsmokers (n = 1586) from March 2019 to July 2019 in Seoul and Cheonan/Asan South Korea using the Fagerström Test Score. Additionally, urine samples (n = 832) were collected for the measurement of urinary nicotine, cotinine, OH-cotinine, NNAL(4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol), CYMA(N-acetyl-S-(2-cyanoehtyl)-L-cysteine), or CEMA (2-cyanoethylmercapturic acid) using LC-MS/MS. The median(interquartile range) nicotine dependence level was not different among the three types of smokers, being 3.0 (2.0-5.0) for TC- (n = 726), 3.0 (1.0-4.0) for EC- (n = 316), and 3.0 (2.0-4.0) for HNBC- (n = 377) only users. HNBC-only users presented similar biomarker levels compared to TC-only users, except for NNAL (HNBC: 14.5 (4.0-58.8) pg/mL, TC: 32.0 (4.0-69.6) pg/mL; p = 0.0106) and CEMA (HNBC: 60.4 (10.0-232.0) ng/mL, TC: 166.1 (25.3-532.1) ng/mL; p = 0.0007). TC and HNBC users showed increased urinary cotinine levels as early as the time after the first smoke of the day. EC users' biomarker levels were possibly lower than TC or HNBC users' but higher than those of non-smokers.

Vaping Cardiovascular Health Risks: an Updated Umbrella Review.

PURPOSE OF REVIEW: Modified risk products (MRP) such as electronic vaping cigarettes (EVC) and heat-not-burn cigarettes (HNBC) are alternatives to traditional combustion cigarettes (TCC) with an expanding consumer base. Yet, their cardiovascular health risks are still unclear. We aimed to summarize the evidence base on this topic by conducting an updated umbrella review. RECENT FINDINGS: We identified 7 systematic reviews, totaling 183 studies and reports, ranging from in vitro and in animal studies to clinical studies in apparently healthy volunteers and patients at risk of cardiovascular disease. Overall, acute EVC use was associated with several toxic effects at molecular, cellular, tissue, organ, and system level. In addition, EVC impacted adversely on blood pressure (BP) management, caused tachycardia, and worsened arterial stiffness. Finally, EVC use was associated with an increased risk of adverse clinical events, including atrial fibrillation and myocardial infarction, even if the causal link is still debated. Most reviews highlighted that the detrimental impact of EVC was of lesser magnitude of that of TCC. In addition, the differential impact of liquids and nicotine was not clearly disentangled. Finally, no review included studies on HNBC. SUMMARY: The present umbrella review suggests that EVC, and likely HNBC, despite clearly causing an increase in overall cardiovascular risk, may represent a temporary lesser evil than TCC in a risk-reduction or risk-modification strategy, aiming for eventual abstinence from all tobacco or nicotine products.

Heat-not-burn cigarettes induce fulminant acute eosinophilic pneumonia requiring extracorporeal membrane oxygenation.

BACKGROUND: Although the cause of acute eosinophilic pneumonia (AEP) has not yet been fully clarified, cigarette smoking is reported to be a risk factor for developing AEP. The heat-not-burn cigarette (HNBC) was developed to reduce the adverse effects of smoke on the user's surroundings. However, the health risks associated with HNBCs have not yet been clarified. We report a successfully treated case of fatal AEP presumably induced by HNBC use. PRESENTATION OF CASE: A 16-year-old man commenced HNBC smoking two weeks before admission and subsequently suffered from shortness of breath that gradually worsened. The patient was transferred to emergency department and immediately intubated because of respiratory failure. Computed tomography showed mosaic ground-glass shadows on the distal side of both lungs with a PaO2/FIO2 ratio of 76. The patient required veno-venous extracorporeal membrane oxygenation (ECMO) for severe respiratory failure. He was diagnosed with AEP by clinical course and detection of eosinophils in sputum; thus, methylprednisolone was administrated. The patient was weaned off ECMO four days after initiation and extubated the day after. He fully recovered without sequelae. CONCLUSION: As far as we know, our patient is the first case of AEP induced by HNBC use successfully treated with ECMO. Emergency physicians must be aware that HNBCs can induce fatal AEP.

Acute eosinophilic pneumonia following heat-not-burn cigarette smoking.

A 20-year-old man was admitted with acute respiratory failure. He had started smoking 20 heat-not-burn cigarettes (HC) per day 6 months previously, then purchased a second device for smoking HC to increase smoking to 40 cigarettes per day 2 weeks before hospitalization. Acute eosinophilic pneumonia (AEP) was diagnosed based on medical history, chest high-resolution computed tomographic findings, and bronchoalveolar lavage fluid eosinophilia. On starting treatment with prednisolone, the patient exhibited complete recovery. A relationship between cigarette smoking and AEP has been suggested. HC were released in September 2015 in Japan, Italy, and Switzerland. HC attract attention as a cigarette generating less harmful substances than a conventional cigarette. We herein report the first case of AEP caused by smoking HC. HC are expected to spread around the world. In the same way as a conventional cigarette, HC should be recognized as a potential cause of AEP.